Table 4.
Cannabinoids anti-cancer potential in CRC.
Phytocannabinoids | Model type | Antitumor effect/mechanism of action | References |
---|---|---|---|
CBG |
in vitro (Caco-2, HCT116) in vivo (athymic nude female mice, xenograft-HCT116; azoxymethane induced colon cancer model) |
Pro-apoptotic, antiproliferative; prompted ROS production, increased CHOP mRNA, increased levels of caspase 3, 7 activity; in xenograft tumors - reduced tumor growth, in AOM tumors – completely suppressed ACF, reduced number of tumors |
(101) |
CBD | (Caco-2, HCT116) in vivo (male ICR mice, AOM induced CRC) |
Antiproliferative; activation of PPAR-γ, TRPV1, CB1R, DNA; protection from oxidative stress, elevated levels of endocannabinoids; the chemopreventive effect in AOM model –reduced number of tumors, ACF, polyps; activated caspase-3, suppressed phospho-Akt protein |
(102) |
in vitro (HCT116 and DLD-1) | Pro-apoptotic; Noxa activation, ROS elevation, induction of ER stress | (103) | |
in vivo (male BALB/c mice, xenograft-CT26) | Anti-angiogenic, antimetastatic; VEGF inhibition | (104) | |
THC | in vitro (SW480, HCT-15, HT29, Caco-2,HCT116, SW620) | Pro-apoptotic; CB1 activation and inhibition of PI3K-AKT, RAS-MAPK cascade, BAD and caspase-3 activation | (106) |